Unmasking the Mimic: Radionecrotic Lesion Masquerading as Brain Neoplasia on Magnetic Resonance Imaging.

Corpus callosotomy is a therapeutic approach for drug-resistant epilepsy, with positive outcomes observed in managing atonic seizures. Despite a decline in its usage, radiosurgical callosotomy remains a viable option for drug-resistant epilepsy due to its low risks of post-radiation neoplasia, albeit not with exceptions. Brain radionecrosis is characterized by tissue death and vascular endothelial damage following the procedure. Despite the low risk of intracranial secondary malignancy associated with radiation in some cases, post-radiation lesions might present with distinct characteristics needing a thorough diagnostic approach. Herein, we present a unique case of a patient with focal epilepsy who developed a radionecrotic lesion following radiosurgical callosotomy, affecting the anterior cingulate cortex, and mimicking a central nervous system (CNS) tumor. Molecular imaging techniques, including 18-fluorodeoxyglucose positron emission tomography/computed tomography (18-FDG PET/CT) and 11C-acetate PET/CT scans, were employed to differentiate the lesion from a tumor. This case underscores the importance of considering radionecrosis as a differential diagnosis in patients who undergo radiosurgical callosotomy presenting with ring-like enhancement lesions on magnetic resonance imaging (MRI).

Frequency and Focus of in Vitro Studies of Microglia-Expressed Cytokines in Response to Viral Infection: A Systematic Review.

It is well known that as part of their response to infectious agents such as viruses, microglia transition from a quiescent state to an activated state that includes proinflammatory and anti-inflammatory phases; this behavior has been described through in vitro studies. However, recent in vivo studies on the function of microglia have questioned the two-phase paradigm; therefore, a change in the frequency of in vitro studies is expected. A systematic review was carried out to identify the microglial cytokine profile against viral infection that has been further evaluated through in vitro studies (pro-inflammatory or anti-inflammatory), along with analysis of its publication frequency over the years. For this review, 531 articles published in the English language were collected from PubMed, Web of Science, EBSCO and ResearchGate. Only 27 papers met the inclusion criteria for this systematic review. In total, 19 cytokines were evaluated in these studies, most of which are proinflammatory; the most common are IL-6, followed by TNF-α and IL-1ß. It should be pointed out that half of the studies were published between 2015 and 2022 (raw data available in https://github.com/dadriba05/SystematicReview.git ). In this review, we identified that evaluation of pro-inflammatory cytokines released by microglia against viral infections has been performed more frequently than that of anti-inflammatory cytokines; additionally, a higher frequency of evaluation of the response of microglia cells to viral infection through in vitro studies from 2015 and beyond was noted.

Association of variants in the ABCB1, CYP2C19 and CYP2C9 genes for Juvenile Myoclonic Epilepsy.

Juvenile myoclonic epilepsy (JME) is the most common of the generalized genetic epilepsies, with multiple causal and susceptibility genes; however, its etiopathogenesis is mainly unknown. The toxic effects caused by xenobiotics in cells occur during their metabolic transformation, mainly by enzymes belonging to cytochrome P450. The elimination of these compounds by transporters of the ABC type protects the central nervous system, but their accumulation causes neuronal damage, resulting in neurological diseases. The present study has sought the association between single nucleotide genetic variants of the CYP2C9, CYP2C19, and ABCB1 genes and the development of JME in patients compared to healthy controls. The CC1236 and GG2677 genotypes of ABCB1 in women; allele G 2677, genotypes GG 2677 and CC 3435 in men; the CYP2C19*2A allele, and the CYP2C19*3G/A genotype in both sexes were found to be risk factors for JME. Furthermore, carriers of the TTGGCC genotype combination of the ABCB1 gene (1236/2677/3435) have a 10.5 times higher risk of developing JME than non-carriers. Using the STRING database, we found an interaction between the proteins encoded by these genes and other possible proteins. These findings indicate that the CYP450 system and ABC transporters could interact with other genes in the JME.